174 resultados para Aggressive


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15 Artists 2014 was a group exhibition of 2D and 3D works held at the Redcliffe City Art Gallery between October 23 - December 6, 2014. My contribution to the group show was a collective series of 10 soft sculptures entitled Organs Without Bodies. These works were composed of latex, plaster, wool, thread, wax and rosin. I seek through my art practice to transform bodily affect into concrete knowledge. My primary motivation can be described as a relational and ethical attempt to find balance between the erotic and the aggressive. These objects are outcomes from an ongoing creative meditation of the simultaneity of dichotomies: inside and outside, cognition and emotion, past and present, connection and differentiation, the erotic and the aggressive. Each of these can be perceived separately with a penetrating focus of attention, yet all are contained within the 'space' of an expansive bodily-felt sense of awareness.

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The Children’s Cancer Institute in Sydney recently launched an ambitious program. From early next year, scientists will analyse the unique cancer cells of 12 children diagnosed with the most aggressive forms of the disease to find the best treatment for each child. By 2020, they aim to have these individualised treatment options available to all children diagnosed with cancers that have a less than 30% survival rate. This way of tailoring treatment to each person is known as personalised medicine, and advances in DNA sequencing have paved the way for a new era in cancer management.

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Understanding mechanisms associated with the emergence of castration resistant prostate cancer cells (CRPC) after androgen deprivation therapy (ADT) is essential to create new therapeutic agents to counteract this aggressive form of prostate cancer (PCa). Because proteases are involved in almost all cancer associated mechanisms such as cell proliferation, invasion and metastasis, we are interested in their modulation in PCa after ADT and their involvement in CRPC.

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Androgen targeted therapies (ATT) are the most commonly used treatments in prostate cancer (PCa).While these therapies are initially effective, PCa cells are able to activate adaptive response pathways to survive these therapies and progress to castration resistant PCa (CRPC), a highly aggressive and ultimately lethal stage of the disease. Neuroendocrine transdifferentiation (NEtD), a process whereby PCa cells gain neuroendocrinelike characteristics, has been implicated in the development of CRPC. The objective of this study is to develop and characterise models of therapy-induced NEtD to investigate the role of this adaptive plasticity in the progression to CRPC.

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Interactions between tumour cells and extracellular matrix proteins of the tumour microenvironment play crucial roles in cancer progression. So far, however, there are only a few experimental platforms available that allow us to study these interactions systematically in a mechanically defined three-dimensional (3D) context. Here, we have studied the effect of integrin binding motifs found within common extracellular matrix (ECM) proteins on 3D breast (MCF-7) and prostate (PC-3, LNCaP) cancer cell cultures, and co-cultures with endothelial and mesenchymal stromal cells. For this purpose, matrix metalloproteinase-degradable biohybrid poly(ethylene) glycol-heparin hydrogels were decorated with the peptide motifs RGD, GFOGER (collagen I), or IKVAV (laminin-111). Over 14 days, cancer spheroids of 100-200µm formed. While the morphology of poorly invasive MCF-7 and LNCaP cells was not modulated by any of the peptide motifs, the aggressive PC-3 cells exhibited an invasive morphology when cultured in hydrogels comprising IKVAV and GFOGER motifs compared to RGD motifs or nonfunctionalised controls. PC-3 (but not MCF-7 and LNCaP) cell growth and endothelial cell infiltration were also significantly enhanced in IKVAV and GFOGER presenting gels. Taken together, we have established a 3D culture model that allows for dissecting the effect of biochemical cues on processes relevant to early cancer progression. These findings provide a basis for more mechanistic studies that may further advance our understanding of how ECM modulates cancer cell invasion and how to ultimately interfere with this process.

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Malignant pleural mesothelioma (MPM) is a rare aggressive cancer of the pleura. Asbestos exposure (through inhalation) is the most well established risk factor for mesothelioma. The current standard of care for patients suffering from MPM is a combination of cisplatin and pemetrexed (or alternatively cisplatin and raltitrexed). Most patients, however, die within 24 months of diagnosis. New therapies are therefore urgently required for this disease. Lysine acetyltransferases (KATs) including KAT5 have been linked with the development of cisplatin resistance. This gene may therefore be altered in MPM and could represent a novel candidate target for intervention. Using RT-PCR screening the expression of all known KAT5 variants was found to be markedly increased in malignant tumors compared to benign pleura. When separated according to histological subtype, KAT5 was significantly overexpressed in both the sarcomatoid and biphasic subgroups for all transcript variants. A panel of MPM cell lines including the normal pleural cells LP9 and Met5A was screened for expression of KAT5 variants. Treatment of cells with a small molecule inhibitor of KAT5 (MG-149) caused significant inhibition of cellular proliferation (p<0.0001), induction of apoptosis and was accompanied by significant induction of pro-inflammatory cytokines/chemokines.

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We have already seen major amendments to Australia’s tax regime to tackle base erosion and profit shifting (BEPS). Several more significant measures were announced in the federal budget, most notably the diverted profits tax, aimed at multinationals which shift tax to a lower taxing jurisdiction. Yet to date, a very simple tax minimisation strategy has been largely ignored in the ongoing reforms and was ignored in the federal budget. Excessive debt loading is a problem that not been afforded the same attention as other aggressive tax planning strategies adopted by multinationals.

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Bees are well known for being industrious pollinators. Some species, however, have taken to invading the nests of other colonies to steal food, nest material or the nest site itself. Despite the potential mortality costs due to fighting with an aggressive opponent, the prospects of a large bounty can be worth the risk. In this review, we aim to bring together current knowledge on intercolony fighting with a view to better understand the evolution of warfare in bees and identify avenues for future research. A review of literature reveals that at least 60 species of stingless bees are involved in heterospecific conflicts, either as attacking or victim colonies. The threat of invasion has led to the evolution of architectural, behavioural and morphological adaptations, such as narrow entrance tunnels, mud balls to block the entrance, decoy nests that direct invaders away from the brood chamber, fighting swarms, and soldiers that are skilled at immobilising attackers. Little is known about how victim colonies are selected, but a phylogenetically controlled analysis suggests that the notorious robber bee Lestrimelitta preferentially attacks colonies of species with more concentrated honey. Warfare among bees poses many interesting questions, including why species differ so greatly in their response to attacks and how these alternative strategies of obtaining food or new nest sites have evolved.

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This submission will address a number of questions raised in section 5.2, “Potential Future Initiatives to target smoking”, of the Healthy Tasmania Five Year Strategic Plan – Community Consultation Draft. Each question has been answered within this submission. This submission will also address the possibility of legal challenges to these proposed changes, a pivotal consideration when implementing any tobacco control laws. This is due to the aggressive nature of the tobacco industry, as illustrated by their attempts to challenge plain packaging laws in the country and through international treaties. The evidence provided in my submission illustrates that prevention of initiation of smoking during adolescence has various benefits in terms of reduction of negative smoking behaviors in later life. I argue that increasing the minimum legal age of purchasing for tobacco to 21 will benefit both the levels of underage smoking as well as the age of onset of initiation of smoking, due to the greater difficulties that those who are underage would experience in accessing tobacco products. I will also address the question of whether the minimum smoking age should be increased to 25.